Dr. Julie, a.k.a. Scientific Chick, brings you insights into what's happening in the world of life sciences. Straight from the scientific source, relevant information you should know about, in plain language.

Sunday, May 24, 2009

I sometimes wish I was a computer science blogger instead of a life sciences blogger. That would mean, or at least should mean, that I know a lot about computers. Unfortunately I’m not a computer science blogger, and I don’t know anything about computers, and that is why I must apologize for the delay leading to this post. Last Friday my computer died on me, dead as could be. I was working on it, got up for a drink (water, as I’m still free from coffee addiction), and when I got back, my trusty laptop had committed suicide (genetic disposition, no doubt). This event caused considerable grief and made me realize that while I am not addicted to coffee, I sure am addicted to using a computer. That being said, I’m back in ComputerLand, and to make up for the delay I am posting about a really, really cool study.

The research paper for today (published May 2009 in Nature) looks at zebra finches, a type of songbird. The song of zebra finches is like a cultural trait: individual finches have small variations in their song and geographically separated finch groups have local song dialects. Overall, though, the song from the zebra finch in the wild (called the “wildtype song”) can be recognized and described. Songbirds learn to sing during their development by being exposed to adult singing males (females lack a singing ability, but at Zebra Finch Idol, they do the judging). This begs the question: What if baby zebra finches aren’t exposed to singing males? To investigate this question, the group of researchers from New York took zebra finch eggs and raised them individually in sound-proof rooms.

A) They never sing.B) They sing normally.C) They sing poorly.D) They spontaneously break out in “A boy named Sue”.

Think about it: if the song is encoded in their genetic code, then it shouldn’t matter whether they are exposed to it or not, and the answer would be B. If the song isn’t encoded in their genetics and they only learn to sing by imitating adult birds, then the answer would be A. D was a red herring, and the correct answer is actually C. The isolated zebra finches sang, but the sound didn’t really resemble the wildtype song.

Good science is all about asking the right questions. Instead of stopping there and analyzing what went wrong, the researchers thought of a really creative way to address the results. They took a second batch of zebra finch eggs (the second generation), and raised them again individually in a sound proof roof, but this time each baby was raised with one adult bird (a singing tutor) from the first generation (the ones who sang poorly). I’ll spare you the quiz this time: the birds from the second generation learned to sing just like their tutors, poorly. However, their song was slightly different. The rhythm and other characteristics of the second generation song were a little closer to the wildtype song. And so the researchers continued: a third generation of birds was raised, this time with second generation tutors. And believe it or not, each generation sang a little more like the wildtype birds and by generation 4, the song was very similar to the original wildtype song.

The conclusion from the article is that song culture is partly encoded in the genetic profile of a population and partly encoded in the environmental variables. Song culture is also a “multigenerational” phenomenon, because it takes a few generations to emerge. It is a bit disappointing that this study doesn’t also look at the mechanisms of what’s happening. For example, song development is known to be associated with something called neurogenesis, which essentially means the birth of new brain cells. Could it be that over a few generations, there is an orderly progression of connections between the new cells? Are the brain cells and associations between brain cells getting reorganized with each new generation? The researchers do promise to look into it, so I’ll stay tuned and keep you posted.

Tuesday, May 5, 2009

Due to the current international media hype on the swine flu, I’ve decided to stray from my usual modus operandi (for those of you just tuning in, my modus operandi is to write about a recent and relevant research article (not a news article!) in the life sciences). Instead of a research article, today I cornered the swine flu and grilled him like it was his PhD thesis defense.

Scientific Chick: What kind of name is swine flu?Swine Flu: It’s a bit funny that I was called swine flu to start with, since I infected humans months before recently taking a liking to pigs in Alberta, Canada. The reason I was called swine flu is because part of my genetic code comes from a flu that usually infects pigs. However, other parts of my genetic sequence come from the avian flu, and some are from the human flu. I guess calling me “human flu” would have been even more panic-inducing. Anyway, I’m not called swine flu anymore, because pork producers thought it would be bad publicity, even though you can’t catch me by eating pork. My new name is the type A H1N1 virus, but I doubt that will stick with the media.

SC: Tell us a little bit about yourself.SF: Well, I’m a virus. That means I’m tiny (about 100 times smaller than your average bacteria), and I’m essentially a collection of RNA segments (which is similar to DNA) and proteins (my machinery to infect you!) encased in an envelope. My H1N1 name comes from the types of proteins on my surface, hemagglutinin (H) and neuraminidase (N). I can only reproduce (for viruses like me, we say replicate) in living cells. When you catch me, I bind to your cells and weasel my way inside. Once inside your cells, my envelope degrades, and my machinery hijacks yours to start making mini-me’s. Once your cell has made a bunch of new viruses, the cell breaks open and releases all the new viruses so they can go and infect more of your cells. Sneaky, huh?

SC: What makes you special?SF: Robert Webster, An American flu virologist, recently dubbed me as a “real super-mixed-up virus”. My genetics are so new and confusing that you don’t have any immunity to me. That’s all part of my plan for world domination.

SC: How fast do you spread?SF: How dare you ask me questions about my reproductive habits? I’m not telling. To find out, you’ll have to analyze my basic reproductive number (R0), which is a variable that describes the number of new infections caused by one infected person.

SC: Will you kill me?SF: Well, you are annoying me with all your questions, but right now I’d have to say no. It’s still unsure whether I will cause severe disease in many people. According to flu researchers, I apparently don’t seem to be anything different than seasonal flu.

SC: Then why did you kill all those Mexicans?SF: I thought you’d ask. You should hear all the theories about this! Some think the Mexicans are more susceptible because of basic hygiene and medical care. Others suggest that air pollution aggravates my symptoms. Some think it’s because of genetic predispositions. But virologists think you shouldn’t jump to conclusions like that. The reality is, compared with Mexico, the number of the people I infected in the USA or in a country other than Mexico is still too small to pick up significant mortality rates, so it’s very hard to compare.

SC: Can we prevent you from infecting us?SF: So far, regular flu-prevention measures apply. Wash your hands, stay away from the coughing sickly-looking person at the office, eat healthy and exercise, and take a deep breath. Should you go out and deplete your local drugstore of its surgical masks stock “just in case”? No, unless you’re a nurse working in the flu ward (and if that’s the case, I’d hope that your masks are provided). Those masks have only been shown to work if infected people wear them (that’s why you see them a lot in Mexico), and are not useful in preventing infection at this stage.

As for vaccines, I happen to know that you’re working hard on developing one. You’re going to have a problem, though. Growing viruses to make vaccines is a slow process, and the world’s influenza vaccine production capacity is limited to about 400 million doses a year. If you want to start making vaccines against me, you’re going to have to sacrifice the making of the regular flu vaccine. A bit of a gamble, isn’t it? Especially considering my seasonal flu brothers are pretty lethal (last year, they killed about half a million people). Good luck figuring that one out.

SC: Can we treat you?SF: I wish I could say I’m indestructible, but I’m no teenager anymore. I’m treatable with two widely-known and used anti-influenza drugs, oseltamivir (Tamiflu) and zanamivir (Relenza), and countries are stocking up.

SC: You’ve been sequenced. What do you say to that?SF: You think you’re so smart, and that because you know all the letters in my genetic code, you know everything about me. You fool! You still don’t know how virulent I am, and what my mutation pattern is.

SC: How did you evade our fancy pandemic prevention plans?SF: I went unnoticed. I was clever and popped up at the end of the regular seasonal flu season, so no one paid attention to me for a while. By the time the World Health Organization and the Center for Disease Control realized what was going on, it was too late to nip me in the bud. Mouahahaha.

SC: Should I panic?SF: One thing is for sure, it seems like the media wants you to panic. Should you give in to the hysteria? Well, it’s good to keep in mind that so far, I’m just like a regular flu. A friend of mine said it best: it’s good to be aware, but there’s no need to be alarmed.

About Me

Dr. Julie is an Assistant Professor of Neurology at the National Core for Neuroethics and the Djavad Mowafaghian Centre for Brain Health at the University of British Columbia. She holds a PhD in Neuroscience.